Abstract
It is well known that oxyhemoglobin and its breakdown products potently catalyze lipid peroxidation (Willis, 1966; Barber and Bernheim, 1967). Following sub- arachnoid hemorrhage (SAH) due to aneurysmal rupture, the subarachnoid space is filled with blood clot, and subsequent erythrocyte lysis leads to the release of oxyhemoglobin. Eventually, cerebral arteries within the subarachnoid space are exposed to oxyhemoglobin and its breakdown products for a considerable length of time. Since the pathogenetic mechanism underlying cerebral vasospasm, a major complication of subarachnoid hemorrhage (SAH) due to aneurysmal rupture has remained elusive despite extensive research efforts, it seems to be a plausible hypothesis that lipid peroxidation triggered by clot lysis is involved in cerebral vasospasm (Asano et al., 1981). We have already shown that the cerebrospinal fluid (CSF) level of lipid peroxides, particularly thiobarbituric acid-reactive substance (TBA-RS), was significantly higher in SAH patients who manifested symptoms of vasospasm than in those who did not (Sasaki et al., 1982). Furthermore, the elevation of the CSF level of TBA-RS in SAH patients was found to be accompanied by a decrease in the CSF level of vitamin E or in the activity of CSF glutathione peroxidase and by a reciprocal activation of serum glutathione peroxidase (Watanabe et al., 1988a). It seems noteworthy that the above alterations in lipid peroxides in the CSF and free-radical scavengers in the CSF or serum became prominent from 4 to 14 days after SAH, concomitant with the occurrence of delayed cerebral vasospasm.
Published Version
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